pubmed-article:20580651 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20580651 | lifeskim:mentions | umls-concept:C0013470 | lld:lifeskim |
pubmed-article:20580651 | lifeskim:mentions | umls-concept:C1704735 | lld:lifeskim |
pubmed-article:20580651 | pubmed:issue | 1-3 | lld:pubmed |
pubmed-article:20580651 | pubmed:dateCreated | 2010-7-12 | lld:pubmed |
pubmed-article:20580651 | pubmed:abstractText | Nesfatin-1 is an 82 amino acid peptide recently discovered in the brain which is derived from nucleobindin2 (NUCB2), a protein that is highly conserved across mammalian species. Nesfatin-1 has received much attention over the past two years due to its reproducible food intake-reducing effect that is linked with recruitment of other hypothalamic peptides regulating feeding behavior. A growing amount of evidence also supports that various stressors activate fore- and hindbrain NUCB2/nesfatin-1 circuitries. In this review, we outline the central nervous system distribution of NUCB2/nesfatin-1, and recent developments on the peripheral expression of NUCB2/nesfatin-1, in particular its co-localization with ghrelin in gastric X/A-like cells and insulin in ss-cells of the endocrine pancreas. Functional studies related to the characteristics of nesfatin-1's inhibitory effects on dark phase food intake are detailed as well as the central activation of NUCB2/nesfatin-1 immunopositive neurons in the response to psychological, immune and visceral stressors. Lastly, potential clinical implications of targeting NUCB2/nesfatin-1 signaling and existing gaps in knowledge to ascertain the role and mechanisms of action of nesfatin-1 are presented. | lld:pubmed |
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pubmed-article:20580651 | pubmed:language | eng | lld:pubmed |
pubmed-article:20580651 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20580651 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:20580651 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20580651 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20580651 | pubmed:month | Aug | lld:pubmed |
pubmed-article:20580651 | pubmed:issn | 1873-1686 | lld:pubmed |
pubmed-article:20580651 | pubmed:author | pubmed-author:TachéYvetteY | lld:pubmed |
pubmed-article:20580651 | pubmed:author | pubmed-author:StengelAndrea... | lld:pubmed |
pubmed-article:20580651 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20580651 | pubmed:day | 9 | lld:pubmed |
pubmed-article:20580651 | pubmed:volume | 163 | lld:pubmed |
pubmed-article:20580651 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20580651 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20580651 | pubmed:pagination | 18-23 | lld:pubmed |
pubmed-article:20580651 | pubmed:dateRevised | 2011-8-10 | lld:pubmed |
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pubmed-article:20580651 | pubmed:year | 2010 | lld:pubmed |
pubmed-article:20580651 | pubmed:articleTitle | Nesfatin-1--role as possible new potent regulator of food intake. | lld:pubmed |
pubmed-article:20580651 | pubmed:affiliation | Department of Medicine, CURE Digestive Diseases Research Center, Digestive Diseases Division UCLA, Los Angeles, CA 90073, USA. | lld:pubmed |
pubmed-article:20580651 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:20580651 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
pubmed-article:20580651 | pubmed:publicationType | Review | lld:pubmed |
pubmed-article:20580651 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:20580651 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |